More on Merciless MRSA Strain

War and Stench: The pandemic that was and yet may be

by Tom Garrett

War and pestilence ride together and there is no better place than an army camp full of recruits, stressed and far from home, for an epidemic to begin. Camp Funston, hastily erected at the outskirts of Ft. Riley, Kansas in 1917 when America entered World War One, was such a place. In March, 1918, recruits had to be diverted from training to help nurse fellow trainees who had fallen ill. The flu spread rapidly. The base hospital and infirmaries were soon overflowing with patients. Outbreaks began in camps elsewhere.

With the warmth of summer, however, the epidemic receded. The soldiers, some still wan and coughing, resumed normal duties. But if the flu virus was forgotten, it was not gone. In September, 1918, the flu returned with a vengeance, beginning in Boston and breaking out in communities across the United States, spreading through the American Expeditionary Force in France, reaching allied and opposing armies, sweeping through the civilian population of Europe and ultimately the world. By the time America’s “doughboys” were home from France, over 43,000, almost as many as had been killed in action, had died from the flu. By the time the pandemic had run its course in the spring of 1920, the global death toll was beyond counting. A conservative estimate is that 40 million died.(1)

Today, ninety-one years later, an offspring of the virus of 1918, quietly residing and mutating in the bodies of pigs whose ancestors evidently contracted it from humans, has reappeared. Few virologists doubt that the swine flu of 2009, though in aging it has changed, finds its birth in the great pandemic.(2) And it is again, as before, conjoined with war. It is a war, as are most, against morality and as are many, driven by avarice. If the global offensive of corporate agriculture, cruel, environmentally devastating, patently unsustainable, is aimed at the natural world and helpless animals rather than directly at fellow humans, its impacts—coming brutally into focus—threaten us all.

Time will tell whether the swine flu of 2009 will return – as did its ancestor – in a ‘second wave,’ to become a global pandemic. We may never know with absolute certainty whether the outbreak of influenza that descended on the village of La Gloria on the plateau east of Mexico City, from mid February to early April was really swine flu or if it came from Granja Carroll, the massive complex of Smithfield Foods hog factories nearby.(3) The villagers, half or more of whom became ill(4) are convinced that they endured exactly the same symptoms later described on TV and equally convinced, after years of suffering from the stench, flies, contaminated water, dysentery, chronic headaches, skin, eye and respiratory infections that are the lot of people the world over who must live near animal factories, that Smithfield was responsible. According to the Mexico City daily, La Jornada, the National Social Security Institute initially supported the theory, suggesting that the clouds of flies could be transporting the virus.

With Big Ag in full damage control mode and the US government and World Health Organization (WHO) obediently renaming swine flu the A(H1N1) flu, Mexican officials have changed their tune. The sows and feeder pigs are said to be “clean”, the workers healthy, the company blameless. The inconvenient fact that the first verified case of swine flu was that of four year old Edgar Hernandez of La Gloria means nothing, say health officials, since 34 other sick people from the village tested negative. Case closed.

But is it? According to La Jornada, covering the outbreak day by day from April 3 to late May, the state run company Birmex, “which used to provide vaccines, serums, immunoglobulins and diagnostic reagents for state public health institutions” was completely dismantled by the (Fox) government preceding that currently in power. “Before Fox” adds Jornada columnist Jaime Avilles, “former president Ernesto Zedilla finished off both the National Institute of Hygene and the National Institute of Virology dedicated to the study of viruses and the development of vaccines.”(5) Hence there was no laboratory in all Mexico that could provide a genetic profile of the new virus and the Ministry of Health was forced, belatedly, to send samples to the National Microbiology Laboratory in Winnipeg, Canada for analysis. The only sample from La Gloria that went to Winnipeg was – apparently at least – that of little Edgar Hernandez. Do thirty four tests by a laboratory that misidentified the H1N1 virus for six weeks or more as the common H2N3 flu virus – there were thousands of cases and a number of deaths before H1N1was identified – really outweigh one verifiable result? The 27 scientists of WHO’s Rapid Pandemic Assessment Collaboration team, including five experts from Mexico, place so little credence in the Ministry of Health’s results that they do not even mention them in Pandemic Potential of a Strain of Influenza A(H1N1): Early Findings, published in Science on May 10. The team relied heavily on analysis of the La Gloria outbreak in assessing the new flu’s pandemic potential.(6)

Unfortunately, the flu had run its course in La Gloria before the WHO group arrived and it did not take blood samples, citing “absence of a specific serological test for the new H1N1 strain”. This left a vacuum that industry wasted no time in filling. Another ‘team’, led by Dr. Carlos Arias, arrived to take blood samples from La Gloria residents and their backyard pigs during the last week in May. This group is largely (if not entirely) funded by the Biotechnology Institute, funded in turn – according to its web site – by “the Merck Company Foundation.” and other pharmaceutical and biotech trade groups with a vested interest in defending industrial animal production. If it is not possible to deny that the villagers suffered from A(H1N1) the intent is to evidently blame it on village pigs, some of whom – given their proximity to people – are almost sure to exhibit antibodies to the virus.(7)

It was difficult for those of us who know Smithfield from hard experience to expect that any investigation that might implicate Granja Carroll would be allowed.(8) The sine quo non of Smithfield chairman Joe Luter’s “formula for success” is political control wherever the company operates. Citizens have blocked roads and defended themselves from the hated company as best they can. Local officials, for the most part, have remained staunch. But there is much evidence, as in Poland, Romania and the United States of high level corruption. The Guardian’s Jo Tuckman found La Gloria residents “afraid to speak openly for fear of retaliation”. One 66 year old villager was hauled away by federal police for agitating against Smithfield; others were threatened. Daily Mail correspondentSharon Churcher, approaching a hog factory complex labeled Site 8-2, saw “an ominous looking compound...with double-perimeter high voltage and razor-wire fences and locked gates...that might be mistaken for a prison—except that the inmates are pigs.” Coming closer, she vomited from the stench of liquefied feces and rotting carcasses. When interviewed, however, health officials and politicians prated the same line: “The farms are operated hygienically as the law requires. The flu could not have begun there”.(9)

Whatever we may (or may not) eventually learn about this H1N1 flu’s emergence, one thing we can be sure of is that factory farming is involved. Swine influenza virus was confirmed in 1930.(10) A similar virus was isolated from a human patient three years later. A vaccine was perfected in 1944 and its use by American pig farmers eventually became routine. For nearly 70 years after the virus was identified, although flu pandemics arose from Southeast Asia in 1957 and 1968, North American pigs were unaffected. Most pigs and about 20% of pig farmers carried antibodies for the “classical” swine flu (which was also designated A(H1N1) but there were less than twenty known cases of humans actually falling ill. In August 1998, however, coughing sows in a Newton Grove, North Carolina hog factory announced the birth of a new virus. Fifty of 2400 affected sows died, hundreds aborted and it was determined that human flu virus had combined – swapped genetic material – with the classical swine virus to form the new strain, designated H3N2.(11)

From that point, the monopoly of classical swine influenza in North America ended.(12) Within a few months the North Carolina virus had gained an avian component, creating the first known triple reassortment (human-swine-avian) flu virus. New viruses, born in the crowded squalor of hog factories and spread across the continent on long distance trucks, appeared almost yearly. No sooner was a vaccine for one strain perfected than another appeared. Some involved further re-combination (reassortment) of RNA from human and swine flu. Some became infective when small mutations (called antigenic drift) in a virus’s AH (hemagglutinin) component that binds to the host animal’s cell membranes and opens the way for the virus to invade, made it unrecognizable to the host’s existing antibodies. A chorus of warnings arose from virologists and epidemiologists that hog and chicken factories were a perfect milieu for generating a new human pandemic. In 2003, the American Public Health Association—the oldest and largest public health organization—found the situation sufficiently dire to call for a global moratorium on factory farms. Their expansion, however, especially in Central and Eastern Europe and Asia, only accelerated.

In seeking a precursor strain to the current A(H1N1) strain, noted science writer Laurie Garrett points to an incident in Wisconsin in 2005 in which a teenager fell ill from an H1N1 flu virus containing human, swine and avian RNA. A “closely matched” strain apparently passed from humans to pigs in 2006 and “caused widespread illness in swine herds, especially in the Midwest.”(13) Others have speculated that one segment of the new virus’s genome came from Southeast Asia. But, although it borrows from earlier strains, the new virus (dare we call it the Mexican flu) is indisputably novel.

Further, it may not be necessary to look far afield to trace its genealogy. It is known that in September, 2008, there was a major outbreak of avian flu in chicken factories located only about 30 miles from Granjas Carroll. The factories are owned by Mexico’s largest producer, Granjas Bachoco, and the outbreak was hushed up to prevent it from impacting Mexican chicken exports. The flu, it seems, spread to chickens in some local villages while sparing others. La Gloria was among those spared; the village of Quechulac, even closer to Granjas Carroll, than La Gloria, was not. Villagers, according to Guardian correspondents on the scene, told them that “An unusual number of chickens died this year on Quechulac. They could not swallow and had white excrement”. Smithfield cites the fact that Quechulac was free of the illness that visited La Gloria (and—less dramatically—other nearby communities) as proof that the flu could not have come from its operations. But might this be a case of what Sherlock Holmes called “The curious incident of the dog in the night”?(14) Might it be that Quechulac was spared the misfortune of La Gloria because the earlier avian flu – chickens in Mexican villages live in close proximity to people – had left inhabitants with antibodies that protected them from the H1N1 virus? This is a mere speculation, to be sure, but it is far from an idle one. A medical team intent on probing the flu’s origin rather than whitewashing Smithfield and the Mexican government will spare no effort to find out whether the nearby avian flu contributed to the subsequent swine flu.

Whatever awaits us, the appearance of the swine flu has served notice, once again, of the interconnectedness of 21st century events. Who could have imagined that the name of a bright eyed four year old in an obscure Mexican village would appear on the pages of newspapers across the planet?

Whatever trajectory the new flu may take, when it has run its course, as it is certain to, other microbial phenomena even more concretely linked to industrial agriculture and factory farms, will not have run their course. They will, very probably, have intensified. The pathogenic contamination of meat is as much a feature of factory farming as the stench that surrounds it and industrial animal production is now recognized as a powerful driver of antibiotic resistance.

The ensuing article on pathogenic contamination and antibiotic resistance is a section drawn from a monograph still in progress. It has been extracted from its unfinished parent and placed separately on the AWI website in part because of the likelihood that the Slaughter-Kennedy “Preservation of Antibiotics for Medical Purposes” bill (HR 1549) may finally make its way through the Congress; in part because of Dr. Tara Smith’s (ongoing) research confirming the presence of Methicilin resistant Staphlococcus aureus (MRSA) in American pigs.(15) The advent of A(H1N1) makes “Pathogenic Resurgence” all the more germane. If there is extreme “second phase” mortality – as in 1918-1919 – from this flu, it will come about, as then, through a lethal combination of virus and bacteria, probably staphylococcus and all too possibly MRSA.(16) As a reader of “Pathogenic Resurgence” will note, the rise of MRSA, most particularly community associated (CA) MRSA, has pandemic potential of its own.

Finally, I would urge the reader to peruse the notes as well as the text, including those in the ensuing section that strive to the shed light on such matters as Shiga toxin and PVL, terms that one can only hope do not, as in the case of H1N1, become household words. I have also, in note (17) done my poor best to explicate some of the terms and acronyms inhabiting discussion of A(H1N1.)

Tom Garrett

June 10, 2009

(1) There is considerable argument as to where the pandemic began but agreement that it finds its origin, one way or another, in World War One. British researchers Oxford, Sefton, Lambkin, et al make a strong case that the flu began on the vast Etaples military camp in northern France in the winter of 1917. They even note “...an additional factor, 24 gases (some of them mutagenic) used in 100 ton quantities to contaminate soldiers and the landscape.” Others cling steadfastly to an American origin in Kansas military camps. No one now believes the “Spanish flu” began in Spain. See: World War One may have allowed the emergence of the “Spanish” Influenza. Oxford, et al, Lancet Inf Dis, Feb, 2002 and A Hypothesis: the conjunction of soldiers, gas, pigs, ducks, geese and horses during the Great War provided conditions for the emergence of the pandemic of 1918-1919. Oxford, et al in Vaccine, Jan 4, 2005.

(2) Kansas State pathobiologist Juergen Richt has worked extensively with both the swine flu virus isolated in 1930 and the reconstructed 1918 flu virus. Late in 2008, he joined with the Canadian National Center for Foreign Animal Disease in Winnipeg to infect pigs (who recovered after mild respiratory infections) with the 1918 virus. Richt finds both the 1930 virus and the current A(H1N1) virus to be direct linear descendents of the virus of 1918. Note: Experimental Infection of Pigs with the Human 1918 Pandemic Virus. Weingardl, Richt, et al Journal of Virology, May, 2009. Also see The pig as a mixing bowl for influenza viruses: Human and veterinary implications Ma, Richt and Kahn Mol Gen Med Jan 2009.

(3) Smithfield Foods, as most people now know, is the world’s largest “pig production” corporation. The Granjas Carroll operation reportedly consists of 72 clusters of hog sheds from which 950,000 pigs – offspring of 56,000 sows – were sent to slaughter in 2008. Interestingly, although Granjas Carroll is often described in the press as 50% owned by Agroindustries Unidas de Mexico, it is not—unlike Norson in Sonora state and Brazilian and Chinese operations—shown as a joint venture in Smithfield’s corporate report.

(4) How many people became ill in/around La Gloria depends upon whose figures are credited. The Mexican press reported 60% of 3000 residents (perhaps in the entire Perote valley) were affected. WHO, taking the figured proffered by the Mexican authorities, assumed “616 cases from a resident population of 1575.” The 2000 census recorded 2290 La Gloria inhabitants.

(6) The WHO team epidemiological model suggests the flu began between November, 2008 and March 2, most probably in January and that the number of Mexican cases, by April 30, ranged between 6,000 and 32,000, with 23,000 carrying the highest probability. The La Gloria result showed the virus focusing heavily on children with 61% of victims under 15 years of age, a trend apparent, but less fully expressed, in the broader population. The teams’ acceptance of the Mexican government’s highly questionable assurance that three village children who died during the outbreak did not die from flu may have biased its mortality estimate downward. The R factor, the average number of persons each flu sufferer transfers his/her virus to, was estimated (during the study period) at 1.2 to 1.4, adequate to sustain an epidemic. Go to: Pandemic Potential of a strain of Influenza A (H1N1): Early Findings. Fraser, Ferguson, et al http://www.scienceexpress.org/ 11 May 2009.

(8) For an illustration of the impunity with which Smithfield operates, see Of Pigs, History and Impunity: Smithfield in Romania, Tom Garrett Animal Welfare Institute Quarterly, Fall, 2007. The company made every effort to cover up an outbreak of Classical Swine Fever – a vastly more serious disease than swine influenza – that broke out in three of its hog factories in July, 2007. Company guards even barred inspectors from entering its sites. Eventually, the miasma from thousands of rotting pigs attracted the press and forced the national government to act exposing the fact that most of Smithfield’s “farms” had been operating in blatant contempt of regulation and law. Visiting the town of Cenei, where the epidemic started, colleagues and I heard hair raising tales. No credibility can be attached to any “investigation” either Smithfield or the Mexican Agriculture Ministry purport to have conducted at Granjas Carroll.

(9) See: Four-year old could hold key in search for source of swine flu outbreak by Jo Tuckman Guardian.co.uk27 April, 2009, and UN team seeks swine flu’s ground zero by Tuckman and E. Carroll Guardian.co.uk 30 April. For a lively, on the scene article, see: The smell is so awful that I start to vomit: Is this farm the Ground Zero of swine flu? by Sharon Churcher at: http://www.dailymail.co.uk/ 5/4/2009.

(10) An excellent paper: Swine, Avian and Human Influenza Viruses by Dr. Ian Brown taken from the OIE/FAO/EU International Reference Library on Avian Influenzais available on www.pighealth.com/influenza.htm. The only theory that fits observed facts it that swine influenza began when the 1918 virus was transmitted to pigs from humans. The disease, although the reconstituted virus is still 100% fatal to rats, was never a serious threat to pigs. Those deliberately infected in 2008 formed antibodies very rapidly and recovered quickly.

(11) A particularly good article, Chasing the Fickle Swine Flu by Bernice Wuethrich appeared in ScienceVol 299 7 March 2003.

(12) Ibid.

(13) The Path of a Pandemic: Laurie Garrett, Newsweek, May 2, 2009.

(14) See: UN team seeks swine flu’s ground zero. Tuchman and Carroll. As for Sherlock Holmes and “The curious incident of the dog in the night:” “But the dog did not bark in the night.” said someone. “That” replied Holmes, “was the curious incident.”

(17) Viruses: In 1884, French microbiologist Charles Chamberlin invented a filter with pores smaller than any known bacteria, making it possible to filter out--completely remove – bacteria from a solution. It was found, however, that a disease producing agent – first thought to be a liquid – could pass through the filter. The unknown agent was called, from Latin, a virus. In 1999, Loefler and Frisch found that even a highly dilute filtered solution from cattle with Foot and Mouth disease could infect other cattle. This established both that the virus was particulate and that it could replicate. In 1906, scientists began growing viruses outside living plants and animals in lymph and diced chicken kidneys. In 1931, Goodpasture grew influenza virus in fertilized chicken eggs. In 1949, in a prodigious breakthrough, John Enders and his associates grew polio virus in cultured human embryo cells opening the way to the development of the Salk polio vaccine, surely among the greatest, and most unreservedly positive, of all medical achievements.

Bacteriophages: There was evidence, as early as 1896, that viruses affected bacteria as well as animals and plants when D.H. Hankin found that a bacteriocidal ‘agent’ small enough to pass through a Chamberlin filter, abounded in the Ganges and Juma rivers. During World War one both British and French researchers confirmed that filterable virus could kill bacteria. In 1917, D’Herelle, at the Pastuer Institute in Paris, announced discovery of an “invisible microbe parasitic on bacteria” and named it, (from the Greek phagein “to eat”) bacteriophage. D’Herrelle subsequently pioneered use of bacteriaphages to treat human infections, and helped found an institute, still operating in Tibilisi, Georgia to study phage therapy and put it into practice. Not all phages, however, are potential friends. Conversion of Vibrio cholerae from a harmless bacteria to a highly virulent pathogen (cholera) is accomplished by a bacteriaphage that injects new genetic material into the bacterium’s genome. There are other examples, several of which are mentioned in ensuing notes. Bacteriophages are now thought to be the most abundant biological entities on the planet.

Electron Microscopes: The very largest viruses, notably Vaccinia, the Cowpox virus from which Smallpox vaccine was derived, are visible as dots through a lens microscope at maximum power of about 2000 magnifications. But scientists knew nothing of viruses’ actual structure until invention of the electron microscope. A lens microscope cannot “see” anything shorter than the minimum wavelength of visible light, about 4-700 nanometers. The wavelength of an accelerated electron, however, is only about 6 picometers, giving an electron microscope 1000 times greater magnification.

Development of the electron microscope (EM), for which Ernst Ruska eventually received a Nobel Prize, began in Germany in 1931. The original “Transmission” (TEM) design came into use after the war. It is, in essence, a tube (early models were up to 6 feet long) maintained as a vacuum to avoid collisions with gas molecules and with a very high voltage electron accelerator, or gun, on one end. The electron beam is focused by an electromagnetic coil, called a “magnetic lens”. After the beam strikes the target,(positioned midway in the tube) electrons that pass through it are refocused and magnified by another lens system and either fall on a photographic plate (as in early models) or on a fluorescent screen from which it can be transferred to a monitor. The image (in common parlance a ‘shadow image’) shows the relative density of every part of the target based on the percentage of electrons that succeeded in passing through. Another kind of EM, perfected later, uses a less intense beam to scan the surface of the target and forms an image from the electrons reflected or scattered by the target rather than those that pass through it. The raster data from the scanning EM (SEM) has less magnification, by about an order of magnitude, than TEM images but gives far more surface detail. Subsequent designs (so far at least) are permutations of these basic systems.

Virions (complete virus particles): The electron microscope opens a window to an unseen universe that is all around us and part of us, but which we had no means—absent technology—of visualizing or even imagining. The first image of a virus, the Tobacco Mosaic virus, came from a prototype EM in the 1939. Since then, it is said that 5000 viruses have been identified and over 2000 categorized. Coming into view, they are seen to range from 10 to around 400 nm in diameter, averaging about one-hundredth the size of a typical bacteria. Plant viruses, including Tobacco Mosaic are chiefly helical, giving them a rod like shape. But most viruses that enter animals (excepting phages and the deadly filoviruses that cause Ebola, Marburg and other hemorrhagic fevers) are spherical and encased in spike like projections. Under EM magnification they look like cockleburs. Most phages have polygonal ‘heads’ containing genetic material, with “sheaths” capable of injecting particles into a bacterium and skinny tail fibers that bind to its surface and then contract to bring the sheath into position. Filoviruses, as much as 1500 nm long but comparatively narrow, somewhat resemble worms.

In 1935, W.M. Stanley succeeded in crystalizing the Tobacco Mosaic virus, revealing that it consists only of ribonucleic acid (RNA) encased in protein and has no independent means of reproduction. Over succeeding decades, as equipment became more sophisticated, scientists learned how viruses enter living cells and use the cell’s resources to replicate themselves. Some co-exist, budding replications out through the cells’ membranes infrequently enough to avoid killing the host cell. Most pathogenic viruses, however – though they may remain dormant inside cells – wind up killing their host, often by lysing(bursting the cell wall). An animal’s defenses – provided the victim lives long enough for T-cell lymphocytes to identify the invader, B-cell lymphocytes to produce antibodies matched to the antigens (proteins on the viruses capsum, or sheath) and for the antibodies to lock to the antigens and neutralize the viruses – can usually overcome an infection. There are exceptions, however. Herpes viruses, among others, can persist for a lifetime and become infective after years of dormancy. The infamous Hepatitis-B virus (which infects hundreds of millions of people) can live for years in a human liver. Liver damage, frequently fatal over time, comes chiefly from the body’s immune response to the virus.

Influenzavirus: The International Committee on the Taxonomy of Viruses recognizes five orders, 93 families and subfamilies and 307 genera, aggregating, at last report, slightly over 2,000 viruses. The family Orthomyxoviridae contains three genera of Influenzaviruses, A, B and C. plus Isavirus and Thogotovirus. Except for Thogotovirus these genera have only one species apiece. While B and C do infect humans (as can T. dhori), all really major outbreaks where the agent is known, including the flu of 1918, have been caused by genus A. The underlying reason why A is more dangerous is that birds (evidently immune to other flu species) as well as pigs and humans are susceptible to it; the immediate reason is that it is highly variable. Unlike other flu species, A contains numerous subtypes.

Influenza A subtypes are classified by the differences in two glycoproteins, hemagglutinin HA (H) and neuraminidase NA (N) that project (bur like) from the viral surface. HA is a complex molecule, containing over 500 amino acids and taking up about a quarter of the virus’s mass. It is a lectin, widespread in nature, that binds to certain sugars and (as one might suspect from its name) has clotting properties. NA, however, contains an enzyme that cleaves sugars. Influenza A is known to disport 16 different versions (subtypes) of H (the “A” is omitted from subtype designations) and nine subtypes of N. Of these H1, H2, H3, H5, occasionally H7 and H9 and possibly H10 are present in viruses that infect humans. These are normally associated with N1, N2 and N3 although bird virus H10N7 is known to have crossed over to heavily exposed humans in Egypt and Minnesota. Thus the designation (A)H1N1 means genus A, hemagglutinin subtype 1, neuraminidase subtype 1. And so on. The majority–probably all–of the 18 known subtype combinations (there are sure to be more) are carried by birds.

The cores of viruses are made up of genetic material. Influenza viruses fall into group 5, one of three groups of viral genomes (out of a total if seven classified by Nobel Prize winning virologist David Baltimore) that are exclusively made up of RNA. The Influenza A genome is a single strand of NRA, divided into eight segments and containing, in the case of the H1N1 subtype, nine proteins and eight genes. RNA genes are less stable than DNA genes and more likely to mutate.

Endocytosis (entry into cells): When an influenza virus comes into contact with an animal cell – say a human epithelial cell in the respiratory tract – the virus’s H spikes find receptors in sialic acid sugar molecules on the cell’s surface and bind to them. At this point the cell is fooled into bringing the intruder inside by a process called endocytosis that cells have evolved to import nutrients, hormones, etc. and carry out other necessary functions. The cell membrane folds inward to form a pit containing the virus, then squeezes the opening together and seals it off leaving the virus in a bubble, or vacuole called an endosome, inside the cell. This is standard procedure, but when the cell begins to digest the contents of the endosome by acidifying its interior, the HA molecule reacts, first by unfolding and releasing a peptide enzyme that locks it to the endosomal wall, then by carrying out a molecular conversion that fuses the endosome to the viral envelope, or capsum. At this point the virus’s M-2 protein opens what is called an M-2 ion channel through the fused wall and releases the contents of the viral core – the viral RNA molecules and accessory proteins – into the cell’s cytoplasm and thence to the host nucleus where the translation and replication are mainly carried out. The cycle proceeds rapidly. Within three hours post infection the host cell’s normal protein synthesis shuts down, and translation of viral messenger (mr) RNA is underway. New progeny virus can be produced within 8-10 hours.

Exocytosis and Apotosis (virion escape and cell death): When a new virion is completed it moves to the cell’s membrane where, except for the secretion from NA molecule, it would be locked to the inner cell wall by the same HA/sugar binding that attached its parent to the outer wall 8+ hours earlier. However, the sialic sugar dissolving enzyme from NA spikes, held back initially, is released, cleaning the sugar from the inside of the host cell membrane and allowing the virion to escape by budding, or exocytosis, that is also routinely practiced by cells. In budding, the cell extrudes material (in this case a new virion) in the same way it imports it, by forming a bubble and sealing the membrane back together behind it. Off goes the virion, spikes projecting from a new phospholipid coat provided by its former host.

How much of this can a cell take before it undergoes apotosis(dies), and how does it die? For all the research lavished on viruses and the enormous body of data available, this does not – in the case of influenza at least – seem entirely clear. It is well known that many influenza viruses can be replicated inside a single cell; at the same time a cell, with its normal regeneration halted, can only endure so much. Japanese scientists suggest that cells that give evidence of abnormality are often engulfed by phagocytes before they lyse.

Defense Against Viruses: Once a virus enters it, a cell’s life, as the saying goes, is likely to be “interesting but brief”. Cells are not, however, internally defenseless; at least not entirely so. A molecule that produces Interferon has been identified in epithelial cells. If it cannot overcome viruses, it can at least inhibit them. Other cytokines may become involved as well; it is theorized that sudden, otherwise inexplicable deaths from the 1918 flu may have been caused by immune overreaction, dubbed “cytokine storms.”

The cornerstone of the immune response is antigen recognition. Certain B-cell lymphocytes mature, with T-cell lymphocite support, as “memory” cells that remember prior antigens and manufacture antibodies to combat them. When a virus with an antigen or antigens that fit existing antibodies shows up, the system makes short work of it. Antibodies lock on to antigens-- in an influenza virus these are the H and N spikes – and neutralize the virion until it can be eaten by a phagocyte. But if the invading virus does not present recognizable antigens, it is another matter. As noted earlier, T-cells must identity the antigen, program B-cells to produce antibodies that fit it and the B-cells must make enough of them to control the infection. Much time can be saved if the new pathogen is closely related to common strains. But if the pathogen is entirely novel it is likely to take more time than the victim has. Mortality from avian flu H1N5 has ranged, depending on time and place, from 60% to over 80%. We can only be thankful that transmission, thus far, has been from birds to humans, not from humans to humans. The same can be said of H10N7, the latest virus to pass from birds to their handlers, which has killed about a third of those infected.

Antigenic Drift, Antigenic Shift and Reassortment: Antigenic drift comes about from minor mutations during replication – usually changes in a few of the amino acids making up the HA antigen – that make the virus unrecognizable to antibodies. This allows the virus to stay a “step ahead” of immune responses, and strains of viruses subject to such ‘mistakes’ are doubtless favored by natural selection. But the advantages conferred by antigenic drift are temporary– immune systems adapt to them quickly – and the pathogen’s virulence, in most cases, is not much changed. Antigenic shift is another matter. This is possible because of the influenza virus’s segmented (eight part) genome. If two genetically distinct viruses of the same genus encounter each other in the same cell, reassortment may occur, in which viruses may exchange, or borrow entire segments (each containing a gene) to produce a new virus. This has occurred with increasing frequency between pigs and turkeys. In 1992, a team led by S.M. Wright compared widely dispersed swine and turkey isolates, finding that swine virus was stable but that 73% of turkey influenza viruses contained genes from swine. Since the outbreak of the virulent H3N2 swine virus in 1998 the situation has become increasingly chaotic, with triple reassortments, viruses combing genes from three sources (often avian, pig and human) are now common and interspecies transmission becoming increasingly frequent. Scientists have created rather hair raising reassortments in the laboratory. These are controlled, but intensive farming is emerging as a vastly larger laboratory that is entirely uncontrolled.

Pathogenic Resurgence

We live in a time of pathogenic resurgence. It is precisely here that a consumer who asks why the corporate blitz of rural America and its pollution and mass abuse of farm animals “has anything to do with me” finds an answer. For as farm animals have been industrialized, foodborne — chiefly meat borne — illness has doubled and redoubled. It is now believed to be five times greater than in 1970. The Centers for Disease Control (CDC) estimate that at least 5,000 Americans die from foodborne pathogens each year, around 325,000 are hospitalized and over 75 million become ill; (1) so called “stomach flu” is more often than not of foodborne origin. While 18th and 19th century scourges, such as typhoid, have been largely eliminated, organisms unknown 30 years ago such as E. coli O157:H7, Listeria monocytogenes, Cyclospora cayetanensus andCampylobacter jejuni have appeared. E -coli O157:H7 made its debut in January 1993 in the Northwest when four children died and 700 more became desperately ill from “Jack in The Box” hamburgers. Kathi Allen, aunt of one of the victims, described the scene:

When I entered the ICU waiting room, the scene was beyond comprehension. Families huddled on plastic mats on the floor. Everywhere you looked you saw the same expression—haunting, frightened faces as family members clung to each other and waited for word on their critically ill children. At times there were as many as 60 people huddled on the floor or in the few coveted chairs...I watched as a woman collapsed when the doctor gathered with family and said, “I’m sorry, we have to take your son’s colon out.” Their son was two. Days later, they would be burying him. I heard the audible gasps as the helicopter whipped the air overhead. They all knew what it meant… another victim was arriving....Then I made the long walk down halls where countless children lay battling for their lives...all because of a hamburger. (2)

Since this disaster — adopting the CDC estimate of an average of 73,000 a year —somewhere in the vicinity of one million more Americans have became ill from E. coli O157:H7, around 30 thousand, mainly children, were hospitalized; at least a thousand died. (3) Hemolytic Uremic Syndrome (HUS)linked to E. coli infections is now the leading cause of kidney failure in children. (4) Few children who become seriously ill from E. coli recover without lasting - sometimes crippling - damage; Guillain- Barre Syndrome is a common aftereffect. This is true of Listeria and the more virulent strains of Salmonella as well. Overall, the Food and Drug Administration (FDA) estimates that 2-3 % of all cases of foodborne illnesses lead to secondary long term illnesses. (5) While Shiga-like toxin carrying E. coli (6) is especially dangerous to children, Listeria, that kills “only” about 500 Americans a year, is lethal to fetuses. Even a mild case, lasting a few hours, can kill an unborn child. (7) The industry and Food Safety and Inspection Service (FSIS) congratulated themselves in 2004 for “marked improvements” in food safety. But S.T.O.P (Safe Tables Our Priority), a national organization founded by mothers of child victims of foodborne illness, reports that the situation deteriorated again in 2007. (8)

It gets worse. As most people know, deaths from antibiotic resistant bacteria have increased dramatically over the past twenty years; the operating rooms and ICUs of many hospitals have become deadly dangerous places. The American Medical Association reported that in 2005, 18,650 Americans — about one in five of those infected — “died from methicillin resistant Staphylococcus aureus (MRSA). (9) Estimates of the overall death toll from antibiotic resistant bacteria vary. The most widely quoted is a report from the Infectious Disease Society of America that estimates around 90,000 people die from bacterial infections annually and that 70%, or 63,000, of these deaths involve antibiotic resistant bacteria. (10) The “final line of defense” against pathogens resistant to other antibiotics is a drug called Vancomycin, so powerful that doctors prescribe it only in extreme cases. Infectious disease specialists, already shaken by the appearance in 2003 of a strain of MRSA virulent enough to penetrate healthy skin, are positively terrified at the prospect of Vancomycin resistant staphylococcus. “Let me tell you this,” writes medical columnist Dr. W.C. Douglas, noting that MRSA deaths in the US already exceed those from AIDS. “The ramifications of a runaway form of antibiotic resistant staph are a lot scarier and more far reaching than AIDS.” (11)

Industrial agriculture can hardly be blamed for antibiotic resistant pneumonia or drug resistant TB. But since the 1950’s, industrial operations have used enormous quantities of antibiotics added to animal feed as growth promoters and to compensate for the execrable conditions under which animals are raised. A preponderance of evidence points to chicken factories, hog factories and cattle feed lots as the Pandora’s boxes in which some of the most dangerous antibiotic resistance has gestated and from which it has spread.

This is certainly true of Salmonella, which sickens at least 1.4 million Americans each year and kills around 100. A sampling of 200 ground meat samples from chicken, turkey, pork and cattle in 2001 showed 20% contamination with the majority of those isolates (84%) displaying antibiotic resistance. The commonest resistant strain (S typhimurium DT 104), 10 times as lethal as ordinary salmonella, now accounts for over a quarter of US Salmonella infections. (12)

Campylobacter, possibly the most common — though fortunately among the least lethal — causes of foodborne illness, with up to 4 million cases each year, showed up in 88% of the poultry samples tested from Minneapolis/St. Paul supermarkets by the Minnesota department of health. (13) A USDA study found that 90% of factory raised broilers carried Campylobacter and that there was a one hundred fold increase in external concentrations of Campylobacter on feathers and exposed skin between testing at broiler factories and arrival at the slaughterhouses. (14)

In 1995 and 1996, FDA’s Center for Veterinary Medicine (CVM), ignoring all protests — even those of Dr Joshua Lederberg who shared a Nobel Prize for discovering that bacteria could exchange genes (including resistant genes) approved two antibiotics of the fluoroquinolone family for use for poultry. As a result Campylobacter is now broadly resistant to the entire spectrum of fluoroquinolone antibiotics including Cipro, the drug of choice in treating it. (15) Infections from resistant strains are more severe than ordinary Campylobacter infections, and more likely to involve bloody diarrhea and require hospitalization. (16)

FDA was eventually forced to defy the industry lobby and reverse its decision. In 2005, after a protracted hearing, approval for Baytril (enrofloxacin) was withdrawn for poultry. (17) Whether the percentage of resistant bacteria will now decline or it is a case of “closing the gate with the horses gone” remains to be seen. But in the meantime, evidence is rapidly accumulating of a linkage between animal factories and the dreaded MRSA.

MRSA was once acquired almost entirely in hospitals or nursing homes, the scourge of surgical and wound patients and persons already seriously ill. But in recent years it has been showing up, sometimes in even more virulent form in outside communities, festering in places like high school locker rooms, afflicting healthy people who have had no contact with hospitals. Community based, or CA-MRSA as it is now called, begins as a skin infection. Most cases — typically puss filled lesions — are treatable but some, usually involving young, previously healthy persons, have been fatal. (18) CA-MRSA is increasing exponentially in certain areas; a study of children in south Texas found a 14-fold increase in cases between 1999 and 2001. (19) A study of Minnesota published in the Journal of the American Medical Association, placed the average age of those afflicted with hospital acquired MRSA (HA-MRSA) at 68 whereas the average victims of CA-MRSA was only 23. (20) Similar trends are underway in Europe. In Denmark, 62% of MRSA cases are now of a community associated (CA) strain and the incidence in children has increased by ten times in as many years. (21)

Despite industry’s stonewalling denials and a “See no evil, Hear no evil, Speak no evil” silence within FDA and USDA, it is now beyond dispute that factory pig farms have become reservoirs of MRSA and that it may be spreading to chicken farms as well.

This first came to light in the Netherlands in 2004 where the Dutch, who have succeeded in keeping hospitals almost entirely free of HA-MRSA, take instant alarm at its appearance. In this case the hospital at Nijmegen unexpectedly found MRSA in postoperative screening cultures of a six month old girl. After learning that the child’s family had not traveled abroad (which is usually how Dutch citizens become MRSA carriers) Dr. A. Voss (22) and his associates investigated further. They found the parents, who were pig farmers were also MRSA positive. In a second case a young mother ill with mastitis proved to be suffering from MRSA. Her husband, a pig farmer, her baby and three workers on their farm tested positive. Eight of ten pigs swabbed at the farm were positive as well. (23) Screening of a group of unrelated pig farmers disclosed that 23% were MRSA positive compared to .03% of the general Dutch population. (24) The Dutch subsequently found pustulous skin infections caused by MRSA in piglets. (25) Tests of 540 pigs at various slaughterhouses revealed that 39% were positive for MRSA. (26) A later study revealed that though live chickens did not appear to carry the strain, no less than 21% of chicken sold in supermarkets tested positive for the bacteria. (27)

The Dutch findings led to surveys elsewhere in Europe. In Belgium, MRSA was isolated among pigs in 68% of the farms visited and in 37% of these cases farmers and their families tested positive. (28) Armand-Lefevre in France found the same distinctive strain of both MRSA and non - resistant staphylococcus aureus in pigs and pig farmers. (29) Comparable results came in from Germany and Austria. (30) In Denmark, almost half of the pigs tested proved positive to the ST 398 strain that had shown up elsewhere in Europe. (31)

Finally, in 2007, testing began in North America. Researchers at the University of Guelph discovered MRSA on 9 of 20 farms surveyed in south - western Ontario. Seventy-one of 285 pigs (25%) and 20% (5 of 25) of pig farmers examined tested positive for MRSA. To the amazement of the investigators, the majority of the colonized pigs and all five farmers carried the European ST398 strain. A few pigs also tested positive for USA 100, the commonest North American hospital strain. About 10% of pork sampled carried the bacteria. (32)

In 2008, Dr. Tara Smith from the University of Iowa, College of Public Health, and her students defied the taboo surrounding the subject to test 209 pigs in regional pig farms. No less than 70% of the animals swabbed were colonized with the ST398 strain and 9 of 20 workers tested positive as well. (33) Despite the numerous cases recorded in Europe (20% of Dutch MRSA infections are ST398 with many serious cases) (34) there is no published record in North America of either human or porcine infections from this strain. However, research so far completed (Dr. Smith is now embarked on a second study) has been limited; samples were collected on only two conventional (factory type) hog farms in the upper mid-west. No one knows or has dared to try to find out — in the long shadow of the powerful industry lobby — what the situation is behind the closed doors of major corporate animal factories and slaughterhouses.

A hint of what may exist behind the curtain came with a local TV report on a CA-MRSA outbreak in a Beltsville, Arkansas chicken hatchery. The following are excerpts from the transcript as it appeared in a subsequent blog. “Everyone in the hatchery has had it,” says Vicki Smith. “They complain about the pain. If they bump (the sores) they almost cry.” There are 32 people in the building and 30 have had it multiple times” says another employee. “You go in every day and you don’t know if you’re going to get to work the next day. There have been people take off five weeks at a time and that ‘s five weeks without income.” “It gets to the point you don‘t want to pick up your kids because you’re scared,” says another. “I work for Pilgrim’s Pride...I have worked in the same place for 32 years” a man writes in response to the show. “I have had MRSA 10 times and have coworkers that had it. I have been scared to go to work for the past year and a half (and) scared to sit down in the break room. We have people take their break in their cars.” (35)

Internet blogs discussing MRSA are often followed by angry, sometimes anguished, first person accounts, often by animal factory employees. “In April” writes a woman who works for a hog factory in Oklahoma, “my husband was hospitalized with MRSA and I with an upper respiratory virus. My daughter was not hospitalized but diagnosed with MRSA with what began as a spider bite. Never had my entire family encountered so many illnesses, until I took this job only 7 months ago. The hogs at the farm had been very ill and very manywere dying...I had never heard of MRSA until my husband’s diagnosis. Only then did I find out that each of our illnesses are most likely from me and my job.” (36)

Does this represent “the tip of a submerged iceberg?” Quite possibly. How long has it been going on? It is well known that animal factory employees are subject to chronic skin, eye, pulmonary and sinus infections. Gail Eisnitz transcribed 800 pages of interviews of South Dakota hog factory workers in 1999. Scores of workers mentioned recurrent skin infections. (37)

While no one disputes that the multiplying strains of MRSA find their origin in antibiotic misuse, there is no absolute proof, even in Western Europe, that farm animal strains were created by feeding antibiotics prophylactically or as growth promoters. Many scientists suspect this but no one really knows where, when or how these strains were born. But the fact that Sweden, that banned sub-therapeutic antibiotics on farms in 1986, has not experienced MRSA in animals and is largely — though not entirely — free of CA-MRSA is highly suggestive. (38) Statistics from elsewhere in Europe, where they have been “sorted” on that basis, show a far smaller percentage of pigs raised on pasture carrying resistant bacteria. In Spain, where 46.51% of all pigs tested were positive for MRSA 398, only about 8% of pigs raised on pasture were carriers. A similar disparity exists between “standard” breeds introduced from outside Spain and native Iberian breeds. (39)

Whatever its genesis, a special strain of MRSA is now resident in a large percentage of European and North American pigs and a modest, but increasing, percentage of cattle. It can infect the animals (though it seems to less often than might be expected), it commonly colonizes humans who work around the animals and it can and does infect people. (40) The bacteria are present on much of the pork sold, reaching 83% in a recent survey of Dutch supermarkets. Worse, as the 398-strain spreads — and it is spreading rapidly in Asia and across the planet — an increasing percentage of the bacteria harbor the Panton-Valentine leucociden toxin (PVL), (41) making it both more dangerous and more virulent.

The denial of the American industry lobby that MRSA 398 strain even exists in the US, or constitutes a problem if it does, can be put in context by recalling that fifteen years ago the Tobacco Institute in Washington, D.C. was still denying that smoking causes lung cancer.

While the industry labels any mention of MRSA in farm animals “hysteria” and government agencies remain obediently silent; another potentially ominous development is gathering momentum. In the mid-1980’s, Enterococcus faecium, a normally innocuous bacterium present in most people’s intestines that occasionally causes infections, was found to have developed resistance to a broad spectrum of antibiotics. A strain called Vancomycin Resistant Enterococcus (VRE) was identified and received startled attention, especially in Europe.

One strain — probably the original strain — of VRE almost certainly owes its existence to routine feeding of Virginiamycin and Avoparcin, antibiotics that bear a close chemical affinity to Vancomycin, to poultry and other farm animals. In their fascinating book The Killers Within, Plotkin and Shnayertson describe how Swedish and Danish scientists made this case with sufficient force to bring EU authorities — despite an industry bias — to a decision to ban agricultural use of antibiotics for other than strictly therapeutic purposes. (42) The ban, preceded by Swedish and Danish bans, came into effect in 2006.

The European ban on antibiotic misuse on farms (the Danish ban has apparently already reduced the percentage of resistant bacteria) will have little effect on events in the US, where Virginiamycin is widely used, or in countries such India and Brazil. The concern is less — at the moment at least — with VRE itself but with what one bacteriologist calls “the disconcerting propensity of Staphlococus aureus to trade genetic material with other bacteria”. (43) It has been known for years that genes conferring Vancomycin resistance can transfer from VRE to MRSA in the laboratory and Vancomycin resistant MRSA has shown up sporadically in hospitals since 1993. It is almost miraculous, given the ubiquity of both MRSA and VRE, and the multiple ways in which genes can be transferred from one genera of bacteria to another, that a full fledged and virulent strain of VRE-MRSA has not emerged.

Ambrose Bierce, the most acid satirist of his age, called war, perhaps more presciently than even he realized “God’s way of teaching Americans geography”. We have had hard lessons in geography since 1913 when Bierce vanished while observing the Mexican revolution. We can only hope that VRE-MRSA does not become “God’s way of teaching Americans bacteriology.”

(3) Centers for Disease Control Division of Foodborne, Bacterial and Mycotic Diseases Reports 2000 through March 27,2008, Foodborne Disease Active Surveillance Network, CDC and other U.S. government data on foodborne illness, however, are surprisingly provisional. CDC estimates are extrapolated from data supplied from only ten states. There is good reason to suspect that Minnesota and Oregon, where the incidence of foodborne disease seems abnormally high, are simply more rigorous in record keeping. Some results strain credulity. In 2007, for example Tennessee reported 79 cases of cases of Shiga toxin carrying E. coli (STEC) and 20 cases of post diarrheal hemolytic uremic syndrome (HUS) in children under 5 years of age; New York reported 70 STEC against only one HUS.

Montreal scientists Bitzan and Riviere in Epidemiological Evaluation of Shiga Toxin producing E. coli (STEC) Infections in the European Community argue, based on HUS cases, that the true incidence of STEC in EU is several times higher than government statistics reflect. If they are correct about EU a similar disparity doubtless exists in the US.

CDC data do, however, make one thing perfectly clear. Despite USDA and industry claims that the situation is improving, the statistics show an upward trend in STEC cases since 2000. The earlier decline in E. coli O157 has been cancelled by a marked increase in STEC from other Shiga toxin carrying E. coli such as O111.

(4) CDC Reports, 2000 through March 27, 2008. For a detailed discussion see: Atcheson, Kare and Keusch in Bacterial Toxins edited by Otto Holst. An encouraging report Patients with E. coli 0157 enterocolitus in the Sakai outbreak by Higami, Nishimoto et al, Osaka Prefecture Medical Association, was recently translated and reprinted in Medline. In this 1996 outbreak, around 5000 children were affected and 122 developed HUS. Most of the victims were administered antibiotics and, in common with US experience, most types proved useless, possibly even deleterious. Subsequent analysis, however, showed that patients given quinolone had a far lower incidence of HUS (3.7% vs 11.6%) than other patients. The authors conclude that “suitable antibiotics can help prevent development of E. coli associated HUS”.

(5) CDC Reports, 2000 through March 27, 2008. The toxin (see note 6), while it is best known for damage to the kidneys and intestinal tract, can attack the eyes and even invade the brain. The fact that CDC estimates of deaths from E. coli do not take into account subsequent mortality from complications of those who survive initial hospitalization means that the real death rate is substantially higher than the official estimate.

(6) Shiga toxin is named for Kiyoshe Shiga, the Japanese physician who identified Shigella dysenteriae in 1898 as the bacteria responsible for a dysentery epidemic that had killed 30,000 people in Japan the previous year. Shigella is now known to be the primary pathogen in the endemic dysentery that ravages the “third world”. In 1903 H. Conradi, discovered a toxin associated with S. dysenteriae. Shiga toxin was subsequently implicated as a cause of hemolytic uremic syndrome (HUS) in humans, and in 1977, Canadian researchers (following earlier work in Japan) found that certain strains of E. coli harbored an almost identical toxin to that found in Shigella. In 1982, a virulent strain of E. coli was identified as the cause of an outbreak of food poisoning. Outbreaks, involving the same strain, E. coli O157-H7, continued through the 1980’s, culminating in the Jack in The Box disaster of 1993. In 2000, virtually the entire population of Walkerton, Ontario—possibly as many as 2500 people—became ill from E. coli contamination of municipal water supply. At least 7 died.

The toxin — apparently inserted into E. coli by bacteriophages — is a protein containing subunits capable of binding to specific receptors on cell surfaces. Since cattle and other farm animals do not have such receptors they are unaffected by the pathogens and shed them in their feces. The vascular epithelium (lining) of human blood vessels, however, does have such receptors and they are particularly numerous in young children.

Thus the toxin, once released in the blood stream, is able to bind to a component of the cell membrane and enter the cell where it combines with the ribosome (RNA) and kills the cell by preventing it from synthesizing protein. The glomerulus — the filtering structure — of the kidneys seems especially vulnerable. Hence bloody diarrhea, the usual symptom of E. coli poisoning, is followed in 5-10% of cases by severe, sometimes fatal, damage to the kidneys and the onset of HUS. A complete discussion of Shiga and Shiga-like toxins is found in Atc zation, Fact Sheet No. 139, 1997. S typhimurium caused the recent outbreak traced to peanut butter from Georgia that killed 8 people and sickened up to 700.

(7) See: Burden and Trends in Listeria monocytogenes M. Patrick in Food Net News — Fall 2008: Volume 2, Issue 4. Personal accounts of fetal death and damage are found in Minimizing & Managing The Risks of Contaminated Food: Ann-Marie McDade, in STOP 2003 Report, page 35 and in What Almost Killed Baby Louise, Elle magazine, April, 2002 by Louisa Kamps. The later deals with an outbreak of listeria from a Cargill turkey plant in Texas that killed four people and resulted in at least three stillbirths. These accounts suggest numerous undiagnosed fetal deaths caused by listeria.

(8) STOP’s contention is supported by CDC tables. After dropping in the late 1990’s, foodborne illness leveled off. Since 2003, which was a statistically “good” year, the trend, overall, has not been favorable. 2007 was a statistically “bad” year.

(17) The Killers Within by Plotkin and Shnayertson, Little Brown, 2002 devotes a full chapter to the struggle by scientists and activists against an industry lobby that had previously dictated FDA policy.

(18) A recent, all too typical account of the death of a teen age athlete from CA-MRSA is found in Jessamine teen’s rapid decline stunned family. Lexington Herald-Leader, http://www.kentucky.com/, March 14, 2009. The youth’s death from CA-MRSA was the third in the Jessamine, Kentucky community in six months. The S. aureus strain was almost certainly USA 300, that typically carries the PVL toxin (see note 41). See: Introduction to MRSA, Medscape.com 11/05/08. Also: USA 300 is dominant CA MRSA Strain in US, excerpted by Staph Watch from Journal o0f Clinical Microbiology. Jan, 2006.

USA 300 is beginning to spread world wide as are other strains of PVL carrying CA-MRSA.

See: Pandemic bug returns as MRSA strain C. Penn, New Scientist, April 1, 2005. Frequent Carriage of PVL Genes by S. aureus isolates from Surgically Drained Abscesses. Issartel, et al, Journal of Clinical Microbiology, July, 2005, p. 3203-3207describes an outbreak in New Caledonia. Prof. K.Y. Yuen, writing in the Hong Kong Medical Diary claims that secondary S. aureus infections were responsible for the high death rate among young soldiers during the 1918 flu pandemic and raises the specter of a new pandemic acting in concert with CA-MRSA. See: CA-MRSA, as an Emerging Public Health Threat. KY Yuen, Hong Kong Medical Diary, December, 2007. Finally, see the review of Australian microbiologist Geoff Coombs from “Down Under” where MRSA first appeared in Molecular Diversity of MRSA in Australia, International Symposium on Staphlocci and Staphlococcal Infections, September, 2006 at http://www.iddi2008.com/.

(37) Ms. Eisnitz conducted these interviews in support of a lawsuit filed against the Bureau of Indian Affairs for permitting a large hog factory on the Rosebud Indian Reservation in South Dakota. She is currently writing a book on the Rosebud outrage. Her interviews may be viewed on the internet at www.hfa.org and proceeding to the entry on South Dakota Hog Factory.

(38) An article documenting decreasing antibiotic resistance after banning antibiotic growth promoters is found at: Antimicrobial Resistance in Scandinavia after a ban of Antimicrobial Growth Promoters: Bengtsson and Wierup, Animal Biotechnology, Vol 17, Nov 2, 2006. The view that CA-MRSA may be linked to animal factories reached The New York Times in Our Pigs, Our Food, Our Health on March 12, 2009 by Op-Ed Columnist Nicholas Kristof.

(40) The rising involvement of MRSA ST398 in human infections and the invasion of ST398 by PVL toxin led respected Dutch researchers Wulf and Voss to pen editorial entitled MRSA in livestock animals—an epidemic waiting to happen, in ClinicalMicrobiology and Infection.

(41) The PVL toxin was discovered in 1894 by Belgian biologist Honore Van de Velde who injected S. aureus into the pleural cavity of rabbits to measure the leukocyte (white blood cell) response. In most cases, the leukocytes increased rapidly and overcame the infection within 24 hours. But some S. aureus isolates contained a “poison” Van de Velde named “leukocidin” that killed white cells and allowed the bacteria to multiply unchecked. (Interestingly, dog leucocytes were unaffected!) In the 1930’s, Panton and Valentine, for whom the toxin is named, found leukocydin at work in 30% of severe human S. aureus infections at London Hospital. With the invention of the electron microscope the character of the PVL toxin came gradually into focus. In 1998 and 2001, the Kamio group at Tohoku University in Japan identified two bacteriophages that rather than lysing (breaking open) the bacteria, inject the PVL into S. aureus by a process known as lysogeny in which the viral genome integrates with the host DNA. When the bacteria come under stress, the viruses lyse their hosts and break out. The viruses kill leucocytes by bonding to their membranes and forming ‘pores’.

In 1995, only a handful of articles on PVL had been published. Since then, as its role in CA-MRSA, and in ever more severe S. aureus infections, has come into focus, around 2000 PVL articles have reached print. For an historical overview, see: A Brief History of Staphylococcus aureus Panton-Valentine leukocidin, Lina, Vandenesch and Eteinne, INSERM EO230, Universite de Lyon.